When diets low in protein, i.e., at or near the requirement for maintenance, are consumed, a thermogenic response is elicited which results in the inefficient utilization of other energy yielding dietary constituents. The phenomenon has been observed in rats, swine and humans. It now seems clear that in some rodents an increase in the activity of brown adipose tissue (BAT) is involved in diet-induced thermogenesis (DIT). BAT is rich in mitochondria whose electron transport system can be readily (but controllably) uncoupled from ATP formation via a specificion conducting pathway mediated by a GDP-binding protein. Although DIT occurs in swine and humans in response to diets low in protein, the role of BAT, if it is even present, is uncertain. Nevertheless, it has been proposed that the same mechanism is involved in DIT in these three species. It is also possible that in the absence of thermogenically active BAT, mitochondrial functions may be altered in other tissues to produce a thermogenic response. Therefore, in order to determine the mechanism(s) of DIT most applicable to humans, the following will be done. BAT-mitochondrial GDP-binding activity will be systematically quantitated in rats fed protein levels ranging from 2 to 60% to demonstrate that at some low level of dietary protein a maximum DIT response is produced without loss of lean body mass and that at some higher level of protein intake the DIT response is minimal. Secondly, because the pig may be an appropriate model for humans a systematic search will be made of the effects of protein intake on the properties of mitochondria prepared from a variety of tissues of swine fed high and low levels of protein in an attempt to elucidate the mechanism(s) of DIT in a species with little or no BAT. The idea that a "low" protein intake leads to the nonconservative utilization of other energy producing, dietary components has appeal vis-a-vis maintenance of ideal body weight inhumans and the success of weight reduction regimens.